The brain contains a renin angiotensin system. Exogenous angiotensin causes hydration changes when injected into a cerebral ventricle. Little information is available on the mechanism by which the brain renin-angiotensin system is regulated. We propose that angiotensin may affect sodium movement into, and within, the brain. To test this hypothesis, we plan to determine if angiotensin affects the kinetics of Na22 transport in choroid plexi. We will also determine if angiotensin levels in cerebrospinal fluid (CSF) change when plasma or CSF sodium levels are altered. Other experiments will determine if CSF sodium concentration is a common mechanism by which osmotic and volume stresses release antidiuretic hormone and cause drinking behavior. These experiments should help define how the brain renin angiotensin system is controlled and thereby help clarify the mechanisms by which this system produces hypertension and salt-water disturbances.